Abstract 2043: Even Minimal Interruptions in Chest Compression for Ventilation Significantly Decreases Coronary Perfusion Pressure

We have previously reported, on the basis of experimental studies, that interruptions of CPR as little as 10 seconds adversely affect the outcomes of CPR. We therefore investigated interruptions of only 5 seconds for delivering ventilation, which corresponds to the current AHA algorithm in which of 30 compressions followed by 2 ventilations are mandated. We hypothesized that even 5 seconds interruption significantly reduces CPP and with significant delay prior to restoring pre-interruption levels. Ventricular fibrillation (VF) was induced and untreated for 15 minutes in 33 male domestic pigs weighting 40±3 Kg. Chest compressions delivered with the aid of mechanical compressor (Thumper, 1000, MI Instruments) with a rate of 100/min. Ventilations were administrated with a compression / ventilation ratio of 30:2 such that 2 ventilations were delivered over a 5 seconds interval. CPP was continuously measured as the difference between comparison diastolic and simultaneous left atrial pressure. CPP significantly decreased during interruptions for ventilation from 20.5±12.8 mmHg to 9.8±6.7 mmHg( P <0.001). After chest compressions were restarted, the CPP increased to 12.5±7.6 mmHg after first compression( P <0.001). A total of 12±7 compressions over a mean interval of 7.2±4.3 seconds was required prior to restoration of CPP to levels corresponding to those that preceded the interruption. As little as the five seconds of interruption in chest compression currently mandated for 30 to 2 ventilations during CPR significantly reduced CPP and delayed restoration of CPP to its pre-interruption level.

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Abstract 17334: The Detrimental Effect of Chest Compression Interruptions on Coronary Perfusion Pressure Dynamics

Circulation ◽

10.1161/circ.132.suppl_3.17334 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Norman A Paradis ◽

Karen L Moodie ◽

Christopher L Kaufman ◽

Joshua W Lampe

Keyword(s):

Blood Flow ◽

Chest Compression ◽

Detrimental Effect ◽

Perfusion Pressure ◽

Vena Cava ◽

Coronary Perfusion Pressure ◽

Right Atrial ◽

Coronary Perfusion ◽

Chest Compressions ◽

Over Time

Introduction: Guidelines for treatment of cardiac arrest recommend minimizing interruptions in chest compressions based on research indicating that interruptions compromise coronary perfusion pressure (CPP) and blood flow and reducing the likelihood of successful defibrillation. We investigated the dynamics of CPP before, during, and after compression interruptions and how they change over time. Methods: CPR was performed on domestic swine (~30 Kg) using standard physiological monitoring. Blood flow was measured in the abdominal aorta (AAo), the inferior vena cava, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical chest compressions (CC) were started after four minutes of VF. CC were delivered at a rate of 100 compressions per minute (cpm) and at a depth of 2” for a total of 12 min. CPP was calculated as the difference between aortic and right atrial pressure at end-diastole per Utstein guidelines. CPP was determined for 5 compressions prior to the interruption, every 2 seconds during the CC interruption, and for 7 compressions after the interruption. Per protocol, 12 interruptions occurred at randomized time points. Results: Across 12 minutes of CPR, averaged CPP prior to interruption was significantly greater than the averaged CPP after the interruption (22.4±1.0 vs. 15.5±0.73 mmHg). As CPR continued throughout the 12 minutes, CPP during compressions decreased (First 6 min = 24.1±1.4 vs. Last 6 min = 20.1±1.3 mmHg, p=0.05), but the effect of interruptions remained constant resulting in a 20% drop in CPP for every 2 seconds irrespective of the prior CPP. The increase (slope) of CPP after resumption of compressions was significantly reduced over time (First 6 min = 1.47±0.18 vs. Last 6 min = 0.82±0.13 mmHg/compression). Conclusions: Chest compression interruptions have a detrimental effect on coronary perfusion and blood flow. The magnitude of this effect increases over time as a resuscitation effort continues. These data confirm the importance of providing uninterrupted CPR particularly in long duration resuscitations.

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Analysis of relation between coronary perfusion pressure and the extracted parameters from a ventricular fibrillation ECG signal

The 26th Annual International Conference of the IEEE Engineering in Medicine and Biology Society ◽

10.1109/iembs.2004.1404114 ◽

2005 ◽

Author(s):

S.J. Jang ◽

J.S. Lee ◽

H.M. Seong ◽

Y.R. Yoon ◽

S.O. Hwang ◽

...

Keyword(s):

Ventricular Fibrillation ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion ◽

Ecg Signal

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Abstract 167: Epinephrine Plus Chest Compressions May Be Superior to Epinephrine Alone in a Hypoxia-Induced Porcine Model of Lifeless Shock

Circulation ◽

10.1161/circ.140.suppl_2.167 ◽

2019 ◽

Vol 140 (Suppl_2) ◽

Author(s):

Felipe Teran ◽

Claire Centeno ◽

Alex L Lindqwister ◽

William J Hunckler ◽

William Landis ◽

...

Keyword(s):

Chest Compression ◽

Porcine Model ◽

Contractile Activity ◽

Coronary Perfusion Pressure ◽

Spontaneous Circulation ◽

Swine Model ◽

Coronary Perfusion ◽

Chest Compressions ◽

Fraction Of Inspired Oxygen ◽

External Chest Compressions

Background: Lifeless shock (LS) (previously called EMD and pseudo-PEA) is a global hypotensive ischemic state with retained coordinated myocardial contractile activity and an organized ECG. We have previously described our hypoxic LS model. The role of standard external chest compressions remains unclear in the setting of LS and its associated intrinsic hemodynamics. Although it is known the patients with LS have better prognosis compared to PEA, it is unclear what is the best treatment strategy. Prior work has shown that chest compressions (CC) when synchronized with native systole results in significant hemodynamic improvement, most notably coronary perfusion pressure (CPP), and hence it is plausible that standard dyssynchronous CC may be detrimental to hemodynamics. Furthermore, retrospective clinical data has shown that LS patients treated with vasopressors and no CC, may have better outcomes. We compared epinephrine only versus epinephrine and chest compression, in a porcine model of LS. Methods: Our porcine model of hypoxic LS has previously been described. We randomized pigs to episodes of LS treated with epinephrine only (control) (0.0015 mg/kg) versus epinephrine plus standard external chest compressions (intervention). Animals were endotracheally intubated and mechanically ventilated, and the fraction of inspired oxygen (FiO 2 ) was gradually lowered from room air (20-30% O 2 ) to a target FiO 2 of 3-7% O 2 . This target FiO 2 was maintained until the systolic blood pressure (SBP) dropped to 30 mmHg for 30 seconds, or the animal became bradycardic (HR less than 40), which was defined as the start of LS. FiO 2 was then raised to 100%, and then animal would receive control or intervention. Return of spontaneous circulation (ROSC) was defined as SBP 60 mmHg, stable after 2 minutes. Results: Twenty-six episodes of LS in 11 animals received epinephrine only control and 21 episodes the epinephrine plus chest compression intervention. The rates of ROSC in two minutes or less were 5/26 (19%) in the control arm vs 14/21 (67%) in the intervention arm (P=0.001;95% CI 19.7 %-67.2%). Conclusions: In a swine model of hypoxia induced LS, epinephrine plus CPR may be superior to epinephrine alone.

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Cardiac Arrest and Resuscitation

10.2310/im.4155 ◽

2015 ◽

Author(s):

Charles N. Pozner ◽

Jennifer L Martindale

Keyword(s):

Cardiac Arrest ◽

Ventricular Arrhythmias ◽

Perfusion Pressure ◽

Pulseless Electrical Activity ◽

Coronary Perfusion Pressure ◽

Spontaneous Circulation ◽

Coronary Perfusion ◽

Chest Compressions ◽

Cardiac Resuscitation ◽

Neurologic Function

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.

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Phase-controlled intermittent intratracheal insufflation of oxygen during chest compression-active decompression mCPR improves coronary perfusion pressure over continuous insufflation

Resuscitation ◽

10.1016/j.resuscitation.2019.02.045 ◽

2019 ◽

Vol 138 ◽

pp. 215-221 ◽

Cited By ~ 1

Author(s):

Kristian Soltesz ◽

Audrius Paskevicius ◽

Henry Pigot ◽

Qiuming Liao ◽

Trygve Sjöberg ◽

...

Keyword(s):

Chest Compression ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion

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Coronary perfusion pressure during external chest compression in pseudo-EMD, comparison of systolic versus diastolic synchronization

Resuscitation ◽

10.1016/j.resuscitation.2012.02.016 ◽

2012 ◽

Vol 83 (10) ◽

pp. 1287-1291 ◽

Cited By ~ 13

Author(s):

Norman A. Paradis ◽

Henry R. Halperin ◽

Menekhem Zviman ◽

David Barash ◽

Weilun Quan ◽

...

Keyword(s):

Chest Compression ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion ◽

External Chest Compression

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Shunting of microspheres across the canine coronary circulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.236.1.h7 ◽

1979 ◽

Vol 236 (1) ◽

pp. H7-H12 ◽

Cited By ~ 2

Author(s):

G. J. Crystal ◽

R. B. Boatwright ◽

H. F. Downey ◽

F. A. Bashour

Keyword(s):

Coronary Circulation ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Left Ventricular ◽

Coronary Perfusion ◽

Blood Samples ◽

Ventricular Afterload ◽

The Difference ◽

Inspired Oxygen ◽

Coronary Sinus Blood

Coronary shunting of 9 +/-1 micrometer and 25 +/- 5 micrometer radiolabeled microspheres was examined in anesthetized, open-chest dogs, whose left common coronary arteries were perfused at controlled pressures. Shunting was estimated from the difference in radioactivity between perfusion line and coronary sinus blood samples during selective elevations of coronary perfusion pressure (CPP), left ventricular afterload, and inspired oxygen. A linear relationship was found between coronary shunting of 9-micrometer microspheres and CPP over the range 100-200 mmHg. According to regression analysis, percent shunt flow was 4.0% at control CPP (100 mmHg) and 10.0% at CPP of 200 mmHg. No shunting of 25-micrometer microspheres occurred at any CPP. Raising afterload did not affect shunting at control CPP but attenuated the increase in shunting at elevated CPP. Changing inspired gas from room air to 100% oxygen did not influence shunting at control or elevated CPP. Raising CPP to 150 and 200 mmHg also released 2.5% and 5.9% of pretrapped 9-micrometer microspheres, respectively. This study demonstrates that vessels permitting passage of microspheres across coronary circulation are sensitive to elevated perfusion pressure.

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Abstract 257: Ventricular Fibrillation Amplitude Spectral Area to Assess the Myocardial Effect of Hemodynamic and Metabolic Interventions During Cardiac Resuscitation in a Rat Model

Circulation ◽

10.1161/circ.140.suppl_2.257 ◽

2019 ◽

Vol 140 (Suppl_2) ◽

Author(s):

Salvatore Aiello ◽

Lorissa Lamoureux ◽

Alvin Baetiong ◽

Jeejabai Radhakrishnan ◽

Raul J Gazmuri

Keyword(s):

Ventricular Fibrillation ◽

Chest Compression ◽

Rat Model ◽

Energy State ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion ◽

Positive Interaction ◽

Cardiac Resuscitation ◽

Spectral Area ◽

Sodium Hydrogen Exchanger

Introduction: The amplitude spectral area (AMSA) of ventricular fibrillation (VF) has been shown to track the myocardial energy state and to predict the effect of defibrillation. We measured AMSA in a rat model of VF and assessed the effects of α-methylnorepinephrine (α-MNE) - a selective peripheral α 2 -adrenoreceptor agonist - given to increase the coronary perfusion pressure without myocardial β 1 -adrenoceptor stimulation and the effects of zoniporide (ZNP) - an inhibitor of the sodium-hydrogen exchanger isoform-1 - given to protect mitochondrial bioenergetic function from reperfusion injury. Methods: VF was electrically induced in 48 rats and left untreated for 8 minutes. Chest compression was then started and defibrillation attempted 8 minutes later. Rats were randomized to receive a 3-mg/kg bolus of ZNP or 0.9% NaCl control (Ctr) before starting chest compression and a 100-μg/kg bolus of α-MNE or 0.9% NaCl control (Ctr) at 2 minutes of chest compression yielding four groups of 12 rats each; ZNP/α-MNE, ZNP/Ctr, Ctr/α-MNE, and Ctr/Ctr. Results: AMSA (mV·Hz; mean±SEM) was 34.9±1.5 at minute one after induction of VF and decreased to 2.6±0.2 at minute eight. With chest compression, AMSA gradually increased attaining different levels among groups (p<0.001). At minute seven of chest compression, AMSA was the highest with ZNP/α-MNE (29.9±2.5; p=0.012 vs Ctr/α-MNE and p<0.001 vs Ctr/Ctr) followed by ZNP/Ctr (24.1±2.5; p=0.016 vs Ctr/Ctr), Ctr/α-MNE (18.9±2.3), and Ctr/Ctr (12.9±2.6). Survival at 240 minutes differed among groups (p=0.007) with the highest survival with ZNP/α-MNE. Analysis of the independent effects of the interventions revealed that AMSA at minute seven was significantly higher with ZNP (27.2±2.6 vs 16.2±1.6; p<0.001) but not with α-MNE (22.9±2.1 vs 18.6±2.8; p=1.000). Survival was significantly higher with ZNP (18/24 vs 7/24; p=0.004) but not with α-MNE (12/24 vs 13/24; p=1.000). Conclusions: AMSA was the highest when ZNP was combined with α-MNE; a combination that also resulted in the highest 240-minute survival. This effect was primarily linked to ZNP without excluding a positive interaction with α-MNE. Accordingly, AMSA may also serve to assess the myocardial effects of metabolic interventions during cardiac resuscitation.

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